Energy consumption associated with fluid and electrolyte transport in the mandibular and parotid glands.

The driving force for Cl- secretion in the salivary acinar cell is believed to be provided by the secondary active uptake of Cl- by Na+ dependent basolateral transporters. The energy cost of primary fluid secretion should therefore reflect the ratio of Na+ entry per mole of Cl- secreted. In the present study, we measured oxygen consumption (QO2) and fluid secretion in perfused mandibular and parotid glands from the rat, and estimated the energy cost of fluid secretion as the ratio of deltaQO2/delta(fluid secretion). During acetylcholine stimulation, the energy cost of fluid secretion by secretory endpieces was higher in the parotid gland than in the mandibular gland. The excess energy cost in the parotid gland may be attributable to other costs than the fluid and electrolyte transport. During bicarbonate-free perfusion in the mandibular gland, bumetanide abolished fluid secretion and QO2 decreased by ca 35%. The remaining QO2 was attributed to Na+ transport activity by basolateral antiports. Assuming values for the energy costs of each transporter and applying these to the total energy cost of the endpieces, the fraction of the total Na+ flux due to Na+/K+/2Cl- cotransport in Na+ handling was estimated to be 0.67. On the other hand, during perfusion with bicarbonate, after subtraction of the bumetanide-sensitive QO2 and the QO2 for antiports, about 19 microl/g/min of QO2 remained, which may be due to activation of Na+/HCO3- cotransport. Thus the inclusion of bicarbonate in the perfusate appears to alter the relative contributions of the various Na+-dependent basolateral transporters to total Na+ handling.